The calibration and use of a calcium ion-specific electrode for kinetic studies of mitochondrial calcium transport

1979 ◽  
Vol 93 ◽  
pp. 430-441 ◽  
Author(s):  
Russell K. Yamazaki ◽  
Donna L. Mickey ◽  
Marianne Story
Keyword(s):  
Calcium Ion ◽  
Calcium Transport ◽  
Kinetic Studies ◽  
Mitochondrial Calcium

scholarly journals ApoE4 (Δ272–299) induces mitochondrial‐associated membrane formation and mitochondrial impairment by enhancing GRP75-modulated mitochondrial calcium overload in neuron

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Tao Liang ◽  
Weijian Hang ◽  
Jiehui Chen ◽  
Yue Wu ◽  
Bin Wen ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Er Stress ◽  
Mitochondrial Dysfunction ◽  
Mitochondrial Function ◽  
Calcium Transport ◽  
Calcium Overload ◽  
Mitochondrial Calcium ◽  
Mitochondrial Impairment

Abstract Background Apolipoprotein E4 (apoE4) is a major genetic risk factor of Alzheimer’s disease. Its C-terminal-truncated apoE4 (Δ272–299) has neurotoxicity by affecting mitochondrial respiratory function. However, the molecular mechanism(s) underlying the action of apoE4 (Δ272–299) in mitochondrial function remain poorly understood. Methods The impact of neuronal apoE4 (Δ272–299) expression on ER stress, mitochondrial-associated membrane (MAM) formation, GRP75, calcium transport and mitochondrial impairment was determined in vivo and in vitro. Furthermore, the importance of ER stress or GRP75 activity in the apoE4 (Δ272–299)-promoted mitochondrial dysfunction in neuron was investigated. Results Neuronal apoE4 (Δ272–299) expression induced mitochondrial impairment by inducing ER stress and mitochondrial-associated membrane (MAM) formation in vivo and in vitro. Furthermore, apoE4 (Δ272–299) expression promoted GRP75 expression, mitochondrial dysfunction and calcium transport into the mitochondria in neuron, which were significantly mitigated by treatment with PBA (an inhibitor of ER stress), MKT077 (a specific GRP75 inhibitor) or GRP75 silencing. Conclusions ApoE4 (Δ272–299) significantly impaired neuron mitochondrial function by triggering ER stress, up-regulating GRP75 expression to increase MAM formation, and mitochondrial calcium overload. Our findings may provide new insights into the neurotoxicity of apoE4 (Δ272–299) against mitochondrial function and uncover new therapeutic targets for the intervention of Alzheimer’s disease.

Inhibition of rat brain mitochondrial calcium transport by chlordecone

1979 ◽  
Vol 51 (1) ◽  
pp. 189-196 ◽  
Author(s):  
David W. End ◽  
Richard A. Carchman ◽  
Richard Ameen ◽  
William L. Dewey
Keyword(s):  
Rat Brain ◽  
Calcium Transport ◽  
Mitochondrial Calcium

Mechanisms of Mitochondrial Calcium Transport

1988 ◽  
pp. 1-14 ◽  
Author(s):  
Thomas E. Gunter ◽  
Douglas E. Wingrove ◽  
Srabani Banerjee ◽  
Karlene K. Gunter
Keyword(s):  
Calcium Transport ◽  
Mitochondrial Calcium

scholarly journals A Kinetic Study of Mitochondrial Calcium Transport

1975 ◽  
Vol 55 (3) ◽  
pp. 497-504 ◽  
Author(s):  
Ken C. REED ◽  
Fyfe L. BYGRAVE
Keyword(s):  
Kinetic Study ◽  
Calcium Transport ◽  
Mitochondrial Calcium

PROTEINS IN MITOCHONDRIAL CALCIUM TRANSPORT

1978 ◽  
pp. 171-186 ◽  
Author(s):  
E. Carafoli ◽  
K. Schwerzmann ◽  
I. Roos ◽  
M. Crompton
Keyword(s):  
Calcium Transport ◽  
Mitochondrial Calcium
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